Kidney Continued Flashcards
1
Q
Water reabsorption in collecting duct
A
- if ADH is present we can draw water out of collecting duct and take away from blood circulation and concentration urine to most concentration
- we need most concentrated - which would be 120 mOsm and can draw water out since osmotic gradient in medulla
2
Q
ADH promotes water reabsorption
A
- act on cells in collecting duct and helps us move water
- ADH - promotes water reabsorption
- ADH/vasopressin - acts on receptor and signal receptor uses cAMP as 2ndary messenger and it stimulates aquaporins (proteins) which move water across these cells so water can be reabsorbed by vasa recta
3
Q
w/out ADH
A
- w/out ADH then filtrate comes in at 100 mOsm and since water isn’t permeable in collecting duct, water just flows thru and get urine of 100 mOsm
- urine not concentrated w/out ADH
- urine osmolarity varies a lot by the state of hydration - dark urine (solutes and very concentrated means not well hydrated)
- ADH release directly related to plasma osmolarity - receptors in hypothalamus
- increase osmolarity and so increase ADH secretion
4
Q
ADH secretion via plasma osmolarity
A
- ADH controls water movemnt and its secretion is a function of plasma osmolarity
- plasma osmolarity is detected by hypothalamus (via osmoreceptors)
- is osmolarity in blood goes up it means your dehydrated and you need to reabsorb water
- vasopressin other function - increase BP via arterial side to increase smooth muscle contraction
- if dehydrated - body water volume goes down, blood vol goes down and bp goes up
- as osmolarity goes up you release ADH since you’re dehydrated and reabsorb more water in kidney and vasopressin acts on arterial side to increase bp since its prob down since dehydrated
- receptor for ADH in blood vessels is diff than cAMP but hormone has that effect
- if well hydrated then don’t release much ADH so not much activity
5
Q
Loop of Henle
A
- descending limb - permeable to water and impermeable to salt
- ascending limb - impermeable to water and moves salt in and out via passive diffusion and active transport via ion pumps
- push salt out and leave water in and dilute what is in the tubule and then create salt gradient on outside in interstitual fluid
- listed by osmolaries
- by pushing salt in ascending limbs we have interstitial fluid w/salt
- sometimes called counter-current multiplier since descending limb and ascending limb make it simplistically lok like moving salt from ascending limb to descending
- what actually happens is what we drew out
- deeper in medulla, the deeper the gradient
6
Q
Vasa Recta
A
- thru the medulla we have the vasa recta that absorbs the water so it doesn’t dilute the salt and any water pulled out of collecting duct if ADH is around and is getting taken away by vasa recta too
- vasa recta is really good at sucking out the water because it has an increase in oncotic pressure
- when we filtered blood in glomerulus, we filtered out sodium, glucose, a.a. and left proteins
- so in that blood continuing to pas in arterioles and PT, it has extra proteins left in which creates extra oncotic pressure which helps w/all absorption
- called counter-current exchanger: free exchange of water and salt
- on descending limb - vasa recta picks up water
- ascending limb - we pick up salt
7
Q
Lasix - loop diuretic
A
- inhibits ion pumps in ascending limb so salt stays in ascending limb and so does water and goes to collecting duct and don’t have proper osmotic gradient
- so salt and water come down and float down into urine so significant way to get rid of excess body fluid
8
Q
Urea Loop
A
- need ADH present for it to work; need stuff in collecting duct to be getting more concentrated since water is being reabsorbed out of collecing duct
- urea gets more concentrated in collecting duct and at bottom increase permeability to urea so it can diffuse out and into interstitial fluid and into ascending limb
- urea in interstitial fluid contributes to osmolarity and helps get to 1200 mOsm when urea loop is working
- osmotic gradient in interstitial fluid is product of loop of henle and urea loop(present w/ADH) both working together
9
Q
Burn victims
A
- problem w/dehydration
- don’t want too much protein because it turns over and produces urea and that has to go into urine and exacerbate things
- so feed then wrong thing due to urea loop and make it worse
- need normal amount of urea from normal protein so get fully concentrated urine
10
Q
Regulation @ glomerulus and distal tubule proximal “juxtraglomerular apparatus”
A
- over wide range of arterial pressure we keep renal plasma flow constant and then keep GFR constant too
- our kidney function regulation is based on GFR stable because everything that nephron does is based on flow rate of nephron to reabsorb properly
- afferent and efferent arterioles can change the diameter to regulate GFR
- reguation via renin cascade
- dilate afferent arteriole then more blood flows in and filtration increases at glomerulus
- if constrict afferent arteriole then less blood flow in and decrease filtration in glomerulus
- if change efferent arteriole:
- constrict - get back pressure in glomerulu and increase filtration temporarily; pressure in PT goes down a bit so more reabsorption
11
Q
Autoregulation
(1) Myogenic mechanism
(2) Tubular-glomerular feedback
(3) Sympathetic Nervous System
A
- myogenic mechanism - intrinsic property of smooth muscle in afferent arteriole which acts like barometer and can measure pressure
- if increase arteriole pressure, smooth muscle response is to increase smooth conctraction so decrease radius, so flow into glomerulus decrease and decrease filtration rate (GFR)
12
Q
Autoregulation -
(2) Tubular-glomerular feedback
A
- way to monitor salts (Na+, Cl- inside tubule)
- special set of cells associated w/distal tubule called macula densa cells and then another set of cells associated w/afferent arteriole and close to distal tubule called juxtaglomerular cells (JG cells)
- renin comes from JG cells and 3 signals to release renin:
- decrease in NaCl in distal tubule
- sympathetic nerves that when stimulate can > renin
- decrease in pressure in afferent arteriole
- renin comes from JG cells and 3 signals to release renin:
- macula densa cells signal JG cells to release renin because they see decrease in Cl- inside tubule, so decrease in GFR since not enough filtration since fluid too much time in tubule
13
Q
Renin Cascade
A
- renin is an enzyme not a hormone
- renin acts on protein angiotensinogen (made in liver and circulates in blood always)
- renin acts on angiotensinogen to make angiotensin I (as it circulates thru lungs) it reacts w/ACE (angiotensin converting enzyme) to make angiotensin II
- angiotensin II: causes vasoconstriction of afferent and efferent arterioles
- low bp due to dehydration, acts on hypothalamus and increase thirst and salt, and hunger and increase ADH
- angiotensin increases aldosterone which is from adrenal gland and increases Na+ retention and K+ excretion
- K+ goes up and then passive channel for K+ goes out and into urine via K+ excretion which is triggered by GFR low or bp low
14
Q
Autoregulation -
(3) Sympathetic NS
A
- If our bp drops really low we can get more intense response via sympathetic NS
- Ex. Hemorrhage: bp really goes down and symp NS response is to decrease GFR and cut down filtration to not make urine temporarily via increase constriction of mesangial cells in glomerulus and so they decrease number of areas that are actually actively filtering so way of decreasing GFR and water volume
- If decrease blood volume and bp falls then respiratory system will increase RMV so baroreceptors pick up that drop in bp; increase CO and HR increases since want to bring bpup and FOC increases so get positive inotropic and chronotropic effects
15
Q
Metabolic Syndrome
A
- visceral fat - makes angiotensinogen so if you have more of it than normal, then make more angiotensin I and II and get all of its actions
- increase thirst, hunger, increase ADH, afferent and efferent vasoconstriction to up your GFR
- bring up body water and more aldosterone and more Na+ and water and blood vol increases so bp increases
16
Q
Macula Densa cells
A
- monitor salt - mostly Cl-
- talk to granular cells
- release renin which gives cascade of renin and angiotensin which has variety of effects
- renin to angiotensin which means we increase aldosterone
17
Q
Aldosterone
A
- Aldosterone gets released and it can be stimulated by renin-angiotensin cascade which itself is due to low bp and low filtration rates
- Boost GFR back up by retaining salt and can do some tricks in the nephron to increase GFR
- Aldosterone released and it will promote: sodium retention and K+ excretion ; activate pump and K+ into lumen of distal tubule
- and since Na+ lowinside P cells of distal nephron we can bring it in and then out to blood via Na-K ATPase pump, and then push K+ out into lumen of distal tubule from blood
•For it to work you need enough sodium in the yellow lumen of distal tubule
18
Q
Aldosterone secretion
A
(1) Renin angiotensin cascade is how aldosterone gets released
(2) Adrenal responds to K+ levels directly which protects us against high potassium (if K+ levels not right then nervous system is out of sorts and easy to have cardiac arrhythmia since electrical system in NS and heart are not right)
- As K+ goes up then make more aldosterone and secrete it and aldosterone lowers K+
- graph is compensatory response showing direct relationship
Other graph – as serum aldosterone goes up you end up excreting more K+
19
Q
Aldosterone Actions
A
- Aldosterone is steroid and attaches to its receptor (mineral corticoid receptor inside the cell cytoplasm and then goes into nucleus and causes changes in gene transcription
- Bind cortisol as well as ald mineral corticoid receptor ; so cells with mineral corticoid receptor also have an enzyme inside the cell and then enzyme takes cortisol and converts to cortisone via 11BHSD2
- cortisone has much decreased affinity for the mineral corticoid receptor and we then metabolize cortisol so it won’t interact with the receptor
